Home - Australian Pharmacist

Once-daily triple therapy for COPD to be PBS listed

Sharon Smith - 5 June 2018

Clinical

A once-daily, single inhaler triple therapy for chronic obstructive pulmonary disease (COPD) is set to be listed on the PBS from 1 July. The...

Symbion PSA Lifetime Achievement Award: Queen of HMRs

David Rowley - 13 October 2020

People

The first woman to win a PSA Lifetime Achievement Award, Debbie Rigby FPS has been many things during her 4-decade career of ‘two halves’.

Aboriginal pharmacy student strives for healthcare equality

Chloe Hava - 26 May 2021

Graduation day: Alexander Burke MPS with Associate Professor Rebekah Moles

Industry

Wiradjuri man Alexander Burke MPS recently graduated from the University of Sydney (USYD) with first class honours. Now, he’s on a quest to change how pharmacy students are taught about Aboriginal and Torres Strait Islander health.

Keeping your cool when vaccinating teens

Chloe Hava - 29 September 2021

Industry

With Spikevax now readily available in pharmacies across the nation, AP has some advice on adjusting your approach to cater for younger patients.

Early elixirs: Amphetamine

Scott Casey - 20 August 2018

Clinical

From wonder drug to scourge. The synthesis of amphetamine has had a profound effect on society as well as attitudes towards drugs. From its use...

Glauber’s salt: the laxative of choice until the 1900s

Dr Leigh Dayton - 12 July 2024

Clinical

Until ‘more sophisticated alternatives’ came about in the 1900s, Glauber’s salt was the global go-to purgative.

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Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

A time sensitive vaccination window

Fear surrounding the vaccination experience

Easing the process

Introduction of FluMist

Training opportunities

Case scenario

Introduction

Learning outcomes

Medicines commonly withheld prior to procedures

Diabetes medicines and peri-procedural blood glucose management

Managing temporary cessation in DAAs

Knowledge to practice

Conclusion

Critical care for vulnerable Australians

Flexibility with hidden costs

Structural barriers

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

A time sensitive vaccination window

Fear surrounding the vaccination experience

Easing the process

Introduction of FluMist

Training opportunities

Case scenario

Introduction

Learning outcomes

Medicines commonly withheld prior to procedures

Diabetes medicines and peri-procedural blood glucose management

Managing temporary cessation in DAAs

Knowledge to practice

Conclusion

Critical care for vulnerable Australians

Flexibility with hidden costs

Structural barriers

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

A time sensitive vaccination window

Fear surrounding the vaccination experience

Easing the process

Introduction of FluMist

Training opportunities

Case scenario